Journal
JOURNAL OF INTERNAL MEDICINE
Volume 290, Issue 3, Pages 632-645Publisher
WILEY
DOI: 10.1111/joim.13298
Keywords
albuminuria; diabetic nephropathy; diabetic retinopathy; remnant cholesterol; type 1 diabetes
Categories
Funding
- Folkhalsan Research Foundation
- Wilhelm and Else Stockmann Foundation
- Medical Society of Finland
- Finnish Diabetes Research Foundation
- Finnish Foundation for Cardiovascular Research
- Liv och Halsa Society
- Waldemar von Frenckell Foundation
- Finnish Kidney Foundation
- Dorothea Olivia, Karl Walter and Jarl Walter Perklen Foundation
- Academy of Finland [316664, 299200]
- Signe and Ane Gyllenberg Foundation
- Sigrid Juselius Foundation
- Novo Nordisk Foundation (NNF) [OC0013659]
- Paivikki and Sakari Sohlberg Foundation
- EVO governmental grant [TYH2018207]
- Academy of Finland (AKA) [299200] Funding Source: Academy of Finland (AKA)
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Remnant cholesterol concentration, but not variability, predicts the progression of diabetic nephropathy and development of severe diabetic retinopathy in patients with type 1 diabetes. However, the causal relationship between remnant cholesterol and these outcomes remains to be elucidated.
Background We aimed to assess whether remnant cholesterol concentration and variability predict the progression of diabetic nephropathy (DN) and severe diabetic retinopathy (SDR) in type 1 diabetes. Methods This observational prospective study covered 5150 FinnDiane Study participants. Remnant cholesterol was calculated as total cholesterol - LDL cholesterol - HDL cholesterol and variability as the coefficient of variation. DN category was based on consensus albuminuria reference limits and the progression status was confirmed from medical files. SDR was defined as retinal laser treatment. For 1338 individuals, the severity of diabetic retinopathy (DR) was graded using the ETDRS classification protocol. Median (IQR) follow-up time was 8.0 (4.9-13.7) years for DN and 14.3 (10.4-16.3) for SDR. Results Remnant cholesterol (mmol L-1) was higher with increasing baseline DN category (P < 0.001). A difference was also seen comparing non-progressors (0.41 [0.32-0.55]) with progressors (0.55 [0.40-0.85]), P < 0.001. In a Cox regression analysis, remnant cholesterol predicted DN progression, independently of diabetes duration, sex, HbA(1c), systolic blood pressure, smoking, BMI, estimated glucose disposal rate and estimated glomerular filtration rate (HR: 1.51 [1.27-1.79]). Remnant cholesterol was also higher in those who developed SDR (0.47 [0.36-0.66]) than those who did not (0.40 [0.32-0.53]), P < 0.001, and the concentration increased stepwise with increasing DR severity (P < 0.001). Regarding SDR, the HR for remnant cholesterol was 1.52 (1.26-1.83) with the most stringent adjustment. However, remnant cholesterol variability was not independently associated with the outcomes. Conclusions Remnant cholesterol concentration, but not variability, predicts DN progression and development of SDR. However, it remains to be elucidated whether the associations are causal or not.
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